Flecainide-Induced Left Bundle Branch Block.

Flecainide is the first-line antiarrhythmic agent used in patients without structural heart disease. It is a class IC antiarrhythmic drug that inhibits inward sodium current through its dose-dependent blockade of voltage-gated calcium channels within the cardiac membrane. It has been shown to slow the conduction in the left bundle branch block. Unmonitored toxicity can cause ventricular dyssynchrony or fatal arrhythmia. We present a case in which flecainide use caused a new left bundle branch block (LBBB).

A Case of Multiple Calcific Embolic Strokes in a Patient With a Porcelain Left Atrium.

Mitral annular calcification (MAC) commonly manifests as an incidental, asymptomatic finding that is associated with several cardiovascular risk factors, atherosclerosis, cardiovascular death, and all-cause mortality. Very rarely, patients with severe MAC can have extensive dystrophic calcification extending into the left atrial wall, termed porcelain left atrium. In this case report, we describe a patient who experienced multiple calcific acute embolic strokes in the setting of severe mitral annular calcification and porcelain left atrium. Our patient presented with multiple, small bilateral acute infarcts scattered throughout the cerebrum and cerebellum confirmed on magnetic resonance imaging (MRI). He was placed on continuous telemetry and underwent multimodal imaging with transthoracic and transesophageal echocardiography, carotid neck ultrasound (US), head and neck computed tomography angiogram (CTA), and cardiac MRI. There were no arrhythmic events detected on telemetry, and all imaging excluded left ventricular thrombi, aortic atheroma, carotid artery stenosis, intracardiac shunting, or large vessel stenosis. Noted on imaging, however, was severe mitral annular calcification with numerous, highly mobile calcific extensions and densely calcified plaque along the posterior left atrial wall, presumed to be the source of this patient's embolic stroke. Cardiac catheterization was significant for severe three-vessel disease requiring coronary artery bypass grafting, and our patient was subsequently discharged to outpatient follow-up on event monitoring and aspirin monotherapy. This case serves to highlight a previously unreported complication of calcific embolic stroke in severe MAC and porcelain left atrium, and highlight the need for further randomized controlled trials to determine the optimum management of these cases.